The broad objective of the proposed study is a more precise definition of potential muscle fatigue mechanisms beyond the traditional claim of neuromuscular junction failure, or depletion of energy supplies. A tentative hypothesis has been made that soium depletion and potassium accumulation in the intercellular spaces (including the t-tubules) appear to interfere with action potential propagation within the muscle cell. Such an occurrence is apparently avoided during maximal voluntary efforts by a natural reduction in the firing frequency of the motor neurons. Confirmation of these arguments will require measurement of electrical activity (the above arguments were formulated on the basis of force measurements alone) from both intact human and isolated curarized animal muscle preparations. Contractile force and muscle electrical activity (smoothed, rectified surface EMG (SRE), and evoked compound surface action potentials (SAP), will be recorded simultaneously during both voluntary and stimulated isometric contractions. Comparison between the results obtained using the two types of contraction (voluntary and stimulated) and between results obtained from the two muscle preparations (intact human and isolated) will allow us to to determine to what extent fatigue is due to failure of: (a) the muscle contractile mechanism, (b) the excitation-contraction coupling process, or (c) neuromuscular transmission and what influence changing behavior of the motor neuron may have on each.